On the Significance of Patient-Specific Systolic Pressure for the Calculation of Rupture Potential Index of Abdominal Aortic Aneurysms

Introduction:: An abdominal aortic aneurysm (AAA) is a dilation of the abdominal aorta characterized by a progressive weakening of the aortic wall. As the AAA diameter increases, so does the risk of rupture, which is a nearly fatal event if the AAA is left untreated [1]. To assess rupture risk, we can utilize computational models that involve patient-specific factors, such as sex, family history, and intraluminal pressure. The objective of this study is to investigate the relative importance of patient-specific mean arterial pressure (PS-MAP) compared to an assumed mean arterial pressure (A-MAP) for the quantification of rupture potential index (RPI) in a sample of symptomatic/ruptured and asymptomatic/unruptured AAAs. This was accomplished by processing computed tomography angiography (CTA) exams from 74 AAA patients performed at Allegheny General Hospital (Pittsburgh, PA) and Northwestern Memorial Hospital (Chicago, IL), which were acquired retrospectively following Institutional Review Board approval at the clinical centers.

Materials and Methods:: The CTA images were segmented from the renal arteries to the aorto-iliac bifurcation using the MATLAB®-based (MathWorks Inc., Natick, MA) script AAAVasc (v1.0.3, The University of Texas at San Antonio) [2], to generate binary images for each image in the CTA stacks with three regions of interest (wall, intraluminal thrombus, and lumen). We used the MATLAB script AAMesh [3] to create volume meshes for each AAA, which were then used to obtain a triangular surface mesh of the AAA wall with patient-specific wall thickness. The surface mesh was used to compute the first principal stress at the wall using nonlinear elastic membrane analysis (NEMA) [4]. The proximal and distal ends of the abdominal aorta were fixed while an intraluminal pressure boundary condition was applied using PS-MAP and A-MAP. The PS-MAP was calculated using the subject’s systolic and diastolic cuff pressures, while A-MAP is a standard 93.33 mmHg. The wall strength was calculated with Eq. (1) [5],

Wall Strength (N/cm²) = 72.9 - 33.5∗(√ILT - 0.79) - 12.3∗(NORD - 2.31) - 24∗HIST + 15∗SEX (1)



where ILT is the ILT thickness (cm), NORD is the normalized local diameter (dimensionless) at each node of the surface mesh, HIST is the familial history of AAA (+0.5 for positive familial history; -0.5 otherwise), and SEX is the sex of the patient (+0.5 for male; -0.5 for female). The RPI was calculated for each element of the surface mesh as the ratio of the first principal wall stress and wall strength.


Results, Conclusions, and Discussions:: The RPI data was organized into groups as follows: G1 and G2 pertain to asymptomatic AAAs (n = 54) for RPI based on A-MAP and PS-MAP (range: 65 mmHg ‒ 175 mmHg), respectively, while G3 and G4 refer to symptomatic AAAs (n = 20) for RPI based on A-MAP and PS-MAP (range: 73.5 mmHg ‒ 183 mmHg), respectively. The maximum RPI values for each group (mean ± standard deviation) are described in Table 1. A t-test was performed (C.I. 95%) to interrogate the validity of the null hypothesis amongst the pairs of AAA groups. Such hypothesis states that the means of the maximum RPI between two AAA groups are equal. Through this analysis, it was determined that there is a statistically significant difference between the maximum RPI of G1 and G2 (p = 0.026). Conversely, there is no statistical significance in maximum RPI between G3 and G4 (p = 0.688), as seen in Fig. 1.

Since statistical significance was demonstrated for the asymptomatic patients, we infer that the patient-specific arterial cuff pressure is necessary to assess AAA rupture potential using a NEMA-based approach for wall stress estimation. Notwithstanding, when a patient is symptomatic there is no incidence in the rupture risk assessment between patient-specific mean arterial pressure and an assumed mean arterial pressure. This latter outcome appears to be counterintuitive, since AAA patients are typically hypertensive such that individual PS-MAP is usually greater than 93.33 mmHg.


Acknowledgements (Optional): : This research was funded in part by NIH award 1R01HL159300.


References (Optional): : [1] Vorp, D. J Biomech, 40(9):1887-902, 2007.
[2] Shum, J. et al., Medical Physics, 37:638-648, 2010.
[3] Raut, S. et al., J Biomech, 48(10), 53:1972-1981, 2015.
[4] Thirugnanasambandam, M. et al., Ph.D. Dissertation, UTSA, 2018.
[5] Vande Geest, J.P. et al., Ann. N. Y. Acad. Sc., 1085:11-21, 2006.